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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four ill or dead desert tortoises (Gopherus agassizii) were received between March 1992 and July 1995 for necropsies from the Mojave and Colorado deserts of California (USA). Diseases observed in these animals included cutaneous dyskeratosis (n = 7); shell necrosis (n = 2); respiratory diseases (n = 7); urolithiasis (n = 3); and trauma (n = 5). In tortoises with cutaneous dyskeratosis the horn layer of shell was disrupted by multiple crevices and fissures and, in the most severe lesions, dermal bone showed osteoclastic resorption, remodeling, and osteopenia. In tortoises with shell necrosis, multiple foci of necrotic cell debris and heterophilic inflammation within the epidermal horn layer were subtended by necrotic dermal bone colonized by bacteria and fungi. Of the seven tortoises with respiratory disease, five were diagnosed with mycoplasmosis. The diagnosis of mycoplasmosis was based on the presence of chronic proliferative rhinitis and positive serologic tests and/or isolation of Mycoplasma sp. Chronic fungal pneumonia was diagnosed in one tortoise with respiratory disease. In the three tortoises with urolithiasis, two were discovered dead, and the live tortoise had renal and articular gout. Traumatic injuries consisted of one tortoise entombed within its burrow, one tortoise burned in a brush fire, two tortoises struck by moving vehicles, and one tortoise attacked by a predator. While the primary cause of illness could be attributed to one or two major disease processes, lesions were often found in multiple organ systems, and a variety of etiologies were responsible for morbidity and mortality.
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PMID:Pathology of diseases in wild desert tortoises from California. 970 60

Excessive specialization and high production requirements place high demands on the metabolism of poultry. A number of metabolic problems, such as disturbances of energy metabolism (affecting mainly hens) and mineral balance (affecting mainly laying hens), affect performance. Nearly all these problems are multifactorial in nature, but diet, and in particular the interaction between diet and phenotype, plays an important role. The problem of ascites in broiler hens is discussed in relation to external and genetic causative factors. Genetic factors can be further subdivided into structural and functional causative factors. This distinction has important consequences. For example, sudden death syndrome can be distinguished as a separate entity. Fatty liver syndrome in laying hens, and gout and urolithiasis in chicks and hens are briefly discussed. Finally, some of the most important or most common skeletal problems affecting poultry, namely, tibial dyschondroplasia, battery fatigue, rickets, and chondrodystrophy, are briefly discussed in the context of the dietary factors that underlie these disorders or which can be used as treatment.
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PMID:[Metabolic insights and nutrition of poultry]. 992 99

Hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency is an X-linked defect of purine metabolism. Clinical manifestations are usually related to the degree of enzyme deficiency: complete HPRT deficiency (Lesch-Nyhan syndrome) presenting with severe neurologic or renal symptoms, or partial HPRT deficiency (Kelley-Seegmiller syndrome) manifesting as a gout-urolithiasis syndrome. A 3-generation kindred is described in which the recognition of partial HPRT deficiency in 2 adolescent male siblings presenting with uric acid lithiasis led to the diagnosis in 2 maternal uncles already in renal failure of unknown cause. This report highlights the importance of clinical awareness leading to early diagnosis, appropriate diagnostic methodology, and therapy of a treatable inherited disorder of purine metabolism for the prevention of renal failure.
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PMID:Partial hypoxanthine-Guanine phosphoribosyltransferase deficiency as the unsuspected cause of renal disease spanning three generations: a cautionary tale. 1177 85

Gout is a common disease arising due to abnormal purin metabolism and excessive accumulation of uric acid in the blood (hyperuricemia) and manifesting with attacks of acute gouty arthritis. In long duration of gout uric acids accumulate in the bones and periarticular tissues as tophuses. Repeat attacks lead to development of chronic gouty arthritis. Purins restriction diet is an important component of gout treatment. Treatment of acute arthritis should be started early, in initial pains before the development of the attacks. Gouty arthritis in the presence of continuous hyperuricemia, tophyses and urolithiasis is treated with allopurinol. Its intake should be long and controlled by the blood level of uric acid. Balneotherapy is recommended for patients with chronic gouty arthritis associated with cardiovascular diseases, urolithiasis.
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PMID:[Gout: current views. Stage oriented treatment]. 1189 31

The kidneys, the bladder and nephrology in general were discussed in the Talmudic literature from their anatomical, pathological and philological aspects. The Sages' deliberations were based on the Biblical texts. The characteristic phraseology of the scriptures uses the kidneys as symbols of the human emotions, contrary to the heart, which is regarded as the location of wisdom. The kidney is considered to be the individual's seat of their deepest desires--perhaps because it is an "internal" organ, well hidden, surrounded by a capsule and by a layer of perinephric fat. The Talmudic corpus considers the kidneys to be the origin of secret counsels--"the kidneys advise". An injury to the kidneys is used symbolically as an example of a cruel and serious injury. The sages were concerned with nephrological problems such as a diseased kidney of small size, fluid and pus in the kidney, injuries, perforations and more. Fascinating advice is given regarding micturition, its timing, characteristics and significance. The Halakhah is concerned with the kidneys during the examination of an animal after slaughter for the fitness for its ritual consumption. The paper presents various nephrological diseases from the Talmudic corpus. Among them are, for example, "Tzemirtha"--urolithiasis; "Hydrakon"--hydronephrosis; "Suskhinta"--urinary retention; "Tzinit"--podagra, gout, and "Yerakon"--icterus. A survey of some Talmudic personalities will exemplify the existence of these conditions.
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PMID:The history of nephrology in the Talmudic corpus. 1209 28

Treatment of asymptomatic hyperuricemia is not necessary in most patients, unless perhaps they have very high levels of uric acid or are otherwise at risk of complications, such as those with a personal or strong family history of gout, urolithiasis, or uric acid nephropathy.
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PMID:Asymptomatic hyperuricemia: to treat or not to treat. 1218 67

There are three stages in the management of gout: (i) treating the acute attack; (ii) lowering excess stores of uric acid to prevent flares of gouty arthritis and to prevent tissue deposition of urate; and (iii) providing prophylaxis to prevent acute flares. It is important to distinguish between therapy to reduce acute inflammation in acute gout and therapy to manage hyperuricaemia in patients with chronic gouty arthritis. During the acute gouty attack nonpharmacological treatments such as topical ice and rest of the inflamed joint are useful. NSAIDs are the preferred treatment in acute gout. The most important determinant of therapeutic success is not which NSAID is chosen, but rather how soon NSAID therapy is initiated. Other treatments include oral and intravenous colchicine, intra-articular and systemic corticosteroids, and intramuscular corticotropin. Optimal treatment of chronic gout requires long-standing reduction in serum uric acid. The urate-lowering drugs used to treat chronic gout are the uricosuric drugs, the uricostatic drugs, which are xanthine oxidase inhibitors, and the uricolytic drugs. Xanthine oxidase inhibitors such as allopurinol, oxipurinol and febuxastat should be used as first-line treatment in patients with renal calculi, renal insufficiency, concomitant diuretic therapy and ciclosporin (cyclosporine) therapy, and urate overproduction. Uricosuric drugs include probenecid, benzbromarone, micronised fenofibrate and losartan. They are the urate-lowering drugs of choice in allopurinol-allergic patients and underexcretors with normal renal function and no history of urolithiasis. The use of recombinant urate oxidase in patients with chronic gout is limited by the need for parenteral administration, the potential antigenicity and production of anti-urate oxidase antibodies, and declining efficacy. The effectiveness of colchicine prophylaxis as an isolated therapy is still to be confirmed by placebo-controlled trials. Another issue is prophylaxis with NSAIDs. There are no comparative studies with colchicine.
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PMID:Management of acute and chronic gouty arthritis: present state-of-the-art. 1548 99

Author presents and analyses informations of non-medical texts of Byzantine historians and chroniclers concerning diseases of Byzantine emperors, concluding that diseases were implicated in certain political and military difficulties. Only one third of the emperors died due to natural causes (i.e. illnesses). Some historians, such as Anna Comnena and Michael Psellos had studied medicine, both of them had excellent knowledge of medical theories of their times. Some diseases in Byzantium were widespread and had high morbidity. This material gives an indication that arthritis (resembling gout) tyrannised a great number of emperors. Contemporary historians maintain that the main causes of gout were overconsumption of alcoholic drinks and food. Other very serious conditions were acute and chronic pyelonephritis and urolithiasis. Relatively frequent conditions of the emperors included pestilential diseases (dysentery, typhoid fever, etc.), psychiatric disorders, epilepsy and arteriosclerosis.
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PMID:[Ill-conditioned rules on the throne of Byzantium]. 1571 71

Hypoxanthine-guanine phosphoribosyl transferase (HPRT) deficiency is an X-linked defect of purine metabolism. Clinical manifestations are usually related to the degree of enzyme deficiency; complete HPRT deficiency (Lesh-Nyhan Syndrome) presenting with severe neurological or renal symptoms, or partial HPRT deficiency (Kelley-Seegmiller syndrome) manifesting as a gout-urolithiasis syndrome. We report a case of partial HPRT deficiency presenting as chronic tophaceous gout, mental retardation, nephrolithiasis and family history suggestive of X-linked inheritance, for its rarity.
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PMID:Partial HPRT deficiency (Kelley-Seegmiller syndrome). 1664 40

Gout refers to heterogeneous group of metabolic diseases characterized by production of deposits of sodium urate crystals in tissues. Gout manifests as acute gouty arthritis with classic clinical picture, or as chronic gouty arthropathy with periarticular and subcutaneous deposits of sodium urate crystals, i.e. tophi. As for kidney, gout is manifested as acute or chronic gouty nephropathy and urolithiasis. These manifestations occur separately or they are combined. Hyperuricemia of primary gout is caused rather by impaired renal secretion than overproduction of uric acid. Secondary hyperuricemia is associated with many pathological conditions; it is also connected with the use of various medicaments. Pathogenesis of gouty arthritis is critically influenced by sodium urate crystals and inflammatory processes they induce. Hyperuricemia is part of metabolic syndrome X which is associated with unanswered question of the relationship between uric acid and atherosclerosis. Although gouty arthritis is the most frequent inflammatory disease of joints in men over 50 years of age, it is often diagnosed and treated inadequately. On that account, the indication of long-term hypouricemic therapy should be always based on the following criteria: secondary causes of hyperuricemia have to be excluded first; frequency of gout attacks and the risk of their recurrence should be taken into consideration; then it is necessary to search for renal manifestations of gout; and last but not least, we should check whether there are any associated diseases classified in metabolic syndrome X.
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PMID:[Pathogenesis, diagnostics and therapy of gout]. 1696 17


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